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What I learnt from talking with Rolf Zinkernagel
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3  4  Next Page Last Page  
 

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Frans
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 Posted: Sat Jul 29th, 2006 08:11

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Owwww, I have looked around a little and see that (most) cells have the MHC molecules that indicate that an invader is present or not, it is simplifying things I know, but do I understand that correctly?

Thank you Trevor.



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Prof Trevor Marshall
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 Posted: Sat Jul 29th, 2006 08:33

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It is simplifying things. Everybody thought we understood the immune system. Thats why you'all are still sick:X

Right now there is focus on what happens inside the cell to signal intracellular pathogens. Virtually nothing is known, although there were recent reports that the nuclear membrane apparently also carries receptors, including TLR (Toll-Like-Receptors).

Russ
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 Posted: Sat Jul 29th, 2006 10:38

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Dr Trevor Marshall wrote: Frans,
I think the MP is like a new boss for the overseer, who retrains him/her to recognize what rot really looks like:)

Is this a permanent retraining?  In other words, once we finish the MP will our immune system be "fixed" so that it recognizes invaders appropriately.  Or is that what the yearly "cleanup" is for?



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jrfoutin
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 Posted: Sat Jul 29th, 2006 10:38

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A clearer understanding of horizontal DNA transfer and just which plasmids get "shared" between host and pathogen, how, and impact of timing and innate immune response for initial transfer and subsequent L-form colonization look like a great new horizon for study to build on the MP foundation. Molecular modeling, in vitro and animal studies like Dr Z's are providing clues, but human in vivo descriptions must be the obvious goal.  

As an aside, all those prenatal vitamins I took for each pregnancy and while I was nursing each child for a year or more do not make me feel great as a mother. Never mind the gallons of milk I chugged or those awful green vitamin drops I gave my babies. Who needed formula for dietary D? I also know both my husband (adopted, formula fed) and I had Th1 symptoms well before we married.

Last edited on Sat Jul 29th, 2006 10:39 by jrfoutin



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Dr. Greg Blaney
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 Posted: Sat Jul 29th, 2006 14:22

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" Any immune response involves, firstly, recognition of the pathogen or other foreign material, and secondly, a reaction to eliminate it"

We know that microbes, especially zoonotic, have sophisticated means to avoid detection.

"Broadly, the different types of immune response fall into two categories: innate ( or non-adaptive ) immune reponses and adaptive immune responses. The important difference between these is that an adaptive immune response is highly specific for a particular pathogen. Moreover, although the innate response does not alter on repeated exposure to a given infectious agent, the adaptive response improves with each succesive encounter with the same pathogen: in effect the adaptive immune system 'remembers' the infectious agent, and can prevent it from causing disease later."
"Phagocytes and innate immune responses - One important group of leucocytes is the phagocytic cells, such as the monocytes, macrophages and polymorphonuclear neutrophils. These cells bind to microorganisms, internalize them and then kill them."

NOT ALWAYS as we know.

"Because they use primitive non-specific recognition systems which allow them to bind to a variety of microbial products, they mediate innate immune response. In effect, they act as a first line of defence against infection."
"In practice there is considerable interaction between the lymphocytes (adaptive immunity) and phagocytes (innate immunity). For example, some phagocytes can take up antigens and show them to T lymphocytes in a form they can recognize, a process which is called antigen presentation. In turn, the T lymphocytes release soluble factors ( cytokines ), which activate the phagocytes and cause them to destroy the pathogens they have internalized. In another interaction, phagocytes use antibodies released by B lymphocytes to allow them to recognize pathogens more effectively. One consequence of these interactions is that most immune responses to infectious organisms are made up of a variety of innate and adaptive components. In the earliest stages of infection, innate response predominate, but later the lymphocytes start to generate adaptive immune responses. They then 'remember' the pathogen, and mount more effective and rapid responses should the individual become reinfected with the same pathogen at a later date."

With this in mind, besides early innoculations with vaccines ( prior to maturation of the adaptive immune system ), the routine use of innate immune suppressing drugs - called anti-inflammatories, anti-pyretic or anti-histamines, for early infections is IMO the major culprit in the epidemic of chronic illness.



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jrfoutin
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 Posted: Sat Jul 29th, 2006 15:54

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"...the innate response does not alter on repeated exposure to a given infectious agent, the adaptive response improves with each succesive encounter with the same pathogen..."

"...most immune responses to infectious organisms are made up of a variety of innate and adaptive components. In the earliest stages of infection, innate response predominate, but later the lymphocytes start to generate adaptive immune responses. They then 'remember' the pathogen, and mount more effective and rapid responses should the individual become reinfected with the same pathogen at a later date."

So are you saying this is why Dr Z's early innoculated mouse died upon subsequent introduction of "similar" infection?

You also suggest pinning down the full complexity of the chronic disease epidemic beyond dietary conditions that create a lush environment for opportunistic pathogens to thrive. Routine use of innate immune suppressing drugs like anti-inflammatories, anti-pyretic, or anti-histimines (as well as to a lesser degree dietary D suppressed innate immune function + ample folate food source in the host) and spreading pathogens with
"early innoculations with vaccines ( prior to maturation of the adaptive immune system )..."
"...Is IMO the major culprit in the epidemic of chronic illness."

Then wouldn't looking at environments that had one of the elements along with chronic disease but not the other might be of some value. (Somewhere that D additives have not been popular, but chronic disease exists because of anti-inflamatories, anti-pyretic,or anti-histimines or the opposite countries that have not used anti-inflammatories, anti-pyretic, or anti-histimines but they do use dietary D and have chronic disease).

Zinkernagel's mouse had no D or anti-etc's? and the onset of death was accute after the second challenge?



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Prof Trevor Marshall
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 Posted: Sat Jul 29th, 2006 16:04

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Janet,
They don't say what the mice were being fed on, but I imagine it was only the best quality pre-packaged mouse-food, and a few minutes searching through Google should reveal the constituents of that (remember this is Swiss mouse-food). I have little doubt it would be fortified, to give the mice a good start in life.

We use only the finest baby frogs, dew picked and flown from Iraq, cleansed in finest quality spring water, lightly killed, and then sealed in a succulent Swiss quintuple smooth treble cream milk chocolate envelope and lovingly frosted with glucose."

"(Monty Python, 'Crunchy Frog' sketch)


That is actually a very good point, you know, Janet:) Google, someone?

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 Posted: Sat Jul 29th, 2006 16:30

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Hmm, it seems to me dr Z. should also test the D-metabolites next time...



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Frans
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 Posted: Sat Jul 29th, 2006 16:56

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Sorry about the last loose canon of a post, now something more serious.

Something occurred to me. The virus dr Z. used was only persistent in the brain, but got killed in the rest of the body by innate immunity. This seems to rule out anything suppressing innate immunity.

Another thought, or question rather, is if it is known if certain parts of the body develop innate immunity earlier than others?  If the brain's innate immunity develops slower, this might account for the susceptibility (of the brain in this instance).

Sincerely, Frans

Last edited on Sat Jul 29th, 2006 16:56 by Frans



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Prof Trevor Marshall
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 Posted: Sat Jul 29th, 2006 17:19

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Frans,
Look at the graph in my FDA presentation slides. You will see that there is a decade of concentrations over which a drug is replaced on a receptor. It is not a simple ON/OFF switch, it is a gradual suppression, which increases with dose.

http://autoimmunityresearch.org/fda_visiting-professor_7mar06.pdf

Also, it is certainly possible that the immune system behaves differently in the brain, and in the rest of the body, at any concentration.

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 Posted: Sat Jul 29th, 2006 17:30

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I may be a slow study, and there are quite alot of things that I did not understand when reading the good doctor's paper, but what I did notice is that he starts off by saying that many autoimmune diseases are precipitated by viral infections. Throughout the paper he continually makes references to viral infections. As such, is he saying that there is a viral component to sarcoidosis? If that is the case, obviously anitbiotics would not help that "portion" of the disease. What are we to make of this paper then and how does it help us?

I am wondering if the cd's will be ready since I would like to see Dr Eishi's theory of sarcoidosis. I am guessing, however, that nobody here believes strictly in Dr. Eishi's work?  It is interesting that many people have had acne problems, but then again, some have not. What are we to make of his findings?

Are we to think that sarc  likely has a 100% bacterial cause, or is there a possibility that there are viral components to this disease?

Lastly, this question might be more appropriate for another area but here goes:

I am on stage 3...d levels still low I suspect, but not much herxing that I can tell - nothing intolerable at any rate. My acne that started after the MP began has stayed pretty much the same, 2 small lesions have developed, and an existing one has stayed exactly the same. Wouldn't we expect them to start to decline (go away) at some point in time?  Why wouldn't we want to up the M just a little ( to say 150 eod)  to see if this helped at all ? I think this is within the normal amts given to teenagers for acne anyway.

Thanks,
Norman

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 Posted: Sat Jul 29th, 2006 17:34

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Sorry...one more question: If there is a viral component to sarcoidosis as the good doctor suggests, are we therefore "S*** out of luck" for a complete cure? I didn't think the body was able to get rid of many of these viruses on its own.

Thanks again,

Norman

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 Posted: Sat Jul 29th, 2006 17:41

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Frans, maybe a 3 arm double blind study?

  • Add D chow on purpose to one group of mice + vaccinate/challenge.
  • The next group anti-inflamatories, anti-pyretic, or anti-histimines + vaccinate/challenge and no D chow.
  • The next just eat D-free lightly killed baby frogs + vaccinate/challenge (hold the glucose).
Dr Marshall, from a simple Google search I found a rodent chow list. From this short list, one can see diet has (*wink*) nothing (*wink*) to do with controlled clinical animal studies. 

Interesting article also turned up by David G. Baker, Natural Pathogens of Laboratory Mice, Rats, and Rabbits and Their Effects on Research (Division of Laboratory Animal Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70810).

Abstract:
Laboratory mice, rats, and rabbits may harbor a variety of viral, bacterial, parasitic, and fungal agents. Frequently, these organisms cause no overt signs of disease. However, many of the natural pathogens of these laboratory animals may alter host physiology, rendering the host unsuitable for many experimental uses. While the number and prevalence of these pathogens have declined considerably, many still turn up in laboratory animals and represent unwanted variables in research. Investigators using mice, rats, and rabbits in biomedical experimentation should be aware of the profound effects that many of these agents can have on research.
..........................

So I'm back at wanting to see some molecular modeling and a little more evidence from human populations. The FDA CPI opportunity 53 of natural history databases, and also compare/contrast of dietary D to anti-histamine and other anti's mentioned by Blaney (OTC?) or combo of both (hello USA!), with mega-analysis data for chronic disease sounds interesting.
..........................

Norman, My understanding is that sarcoidosis and other Th1 diseases respond to the MP because the innate immune system becomes enabled. The exact pathogen or complexity of pathogens and layering of pathoghens over time vary. Some have more bugs per square inch maybe. I can think of several ph3 folks besides myself that still have skin Herxing from time to time and ongoing. It takes time.

Last edited on Sat Jul 29th, 2006 18:11 by jrfoutin



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Prof Trevor Marshall
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 Posted: Sat Jul 29th, 2006 17:56

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Norman,
Once the Th1 bacterial pathogens are killed off, the immune system deals with the viruses it couldn't clear while the bacteria were present. That's why folks lose warts, psoriasis, and other things as they recover on the MP. Relaaaaax...

norman
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 Posted: Sat Jul 29th, 2006 18:21

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LOL.........thanks for the quick response. You always seem to zing me ! LOL !

rick
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 Posted: Sat Jul 29th, 2006 19:30

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  Reenie wrote:” I wonder how much help that one day gave sis' immune system over mine.  I always seemed to be more sickly than my sis.”  

 Jrfoutin wrote; “Who needed formula for dietary D? I also know both my husband (adopted, formula fed) and I had Th1 symptoms well before we married.”  

I find the above two quotes similar to my experience and observations, I was adopted in the nineteen fifties and was taken away from my birth mother at birth.

What I find interesting is that for the first 7-8 years of my life I remember nothing but pain in my bones, primarily the legs and feet which I would describe now as like piano wire being pulled through the marrow.

I know my adoptive parents took me to specialist after specialist with no reasonable explanation for this pain. I remember asking later in life; did they ever think that perhaps this could have been because I was deprived of Colostrum at birth and did this give me a predisposition to a deprived immune system?  The answer of course was no because I was supplemented with formulas etc. My adoptive mother confirmed I was supplemented with Vitamin D because of the severe aching in the bones.

Later in life I met my birth mother and four siblings, two children stayed with her and the other two were also adopted out, guess which three have Th1 illness now? Coincidence?

Does this suggest that the immune system is genetically predisposed to these illnesses later in life because of being colostrum deprived in those first few days? Or perhaps the c-jun gene does remain active after our bodies have developed instead of staying dormant, or even reawakens in the event of pathogen challenges we acquire over the next 40 years.

What Trevor says about it not being one specific pathogen but a host of pathogens acquired over a lifetime including some just being “at the scene of the crime”, that statement is ringing in my ears!     

Maybe acquisition started from day 1. 

                                                  Rick 



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 Posted: Sun Jul 30th, 2006 02:39

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Trevor - John and I have been reading this thread with much interest, particulary when you say:

Now if certain bacterial species were able to persistently infect the neo-natal brain in the same way as Rolf's CMV did, then it could be expected that those folk might well experience a greater degree of difficulty clearing a challenge later in life, just like the mice did... Hmmm...


We thought you might be interested in hearing about the first few weeks of Matt's life nearly 14 years ago.....

Matt was 5 weeks premature and spent his first few days in a humidicrib.  I breast-fed him but he was supplemented with formula and was given quite a few feeds with a tube.  We were in hospital for 10 days and then allowed home once he was OK out of the humidicrib and I had established his feeding and he was over a bit of jaundice (my memory is a bit hazy but that is the jist of it). 

All was well for a few days until he started sleeping through feed times.  I got worried and called our pediatrician - to cut a long story short, he ended up in the neonatal intensive care unit for 10 days and tested for all kinds of things.  He stopped breathing a couple of times that night we took him to hospital, but he was revived each time and put on a cocktail of antibiotics while they tried to work out what was wrong.  He responded favourably to the antibiotics and we were later told that he had an E. coli urinary tract infection that ended up in sceptacemia.  He probably picked up the infection in hospital (I always worried about that tube-feeding...).

We have always wondered why, out of the 1600 boys in Matt's school, he is the only one in recent momory who has missed a couple of years of schooling due to a chronic disease.  We are sure he is not the only one to be bitten by an insect or tick in the Canberra/South Coast region in the past few years.  Sure, the school has its share of autistic kids and others with asthma and ADD, but none with an illness like Matt's that has put him out of action for such a long period of time.  Matt keeps asking, "Why me?" - do you think we may be beginning to find an answer for him??? 

Regards, Robyn and John



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norman
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 Posted: Sun Jul 30th, 2006 07:48

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Trevor,

Just an FYI that I wasn't upset in the least last night, just a bit confused. I think it's sometimes hard to judge a person's thoughts without speaking to him, and that often leads to misunderstandings :o).

I would still like to know if I can find any of Dr. Eishi's work anywhere so I can look at it. It does seem, however, that you would be leaning to a combination of bacteria and viruses as a combined force causing the immune reaction of sarc.

I understand the position that you are trying to reset the immune response, but here's my question that I am fuzzy about:  With respect to  my acne breakout and newly developed lesions since starting the MP , and ( i believe) a stronger herx reaction when I previously ( and mistakenly I will admit) took a greater than recommended dose of minocycline, why would you not suggest taking a larger dose if a person could handle it and it was under the recommended dosage of the drug given to teenagers for acne?  It's just that it seems to me if the doctor is perscribing a certain dosage to teenagers, why would one think a much lesser dose would work just as well or better?  Would taking more M somehow lessen the degree to which the MP works in some way? Would taking any topical medications help?

I am not sure what relation this acne breakout and the two newer skin lesions (about the size of your pinky nail) has to do with my sarcoidosis...whether it's a large part of the cause (the primary cause) or if there are many other bacterial and viral infections going on, but I'm wondering if at least trying to hit the acne would help somewhat? Lastly, would you take the acne breakout ( which has not resolved in a year or more) and the skin lesions as a good sign ...possibly a sign that the bacteria is not "comfortable" remaining in hiding...or that the immune system is now responding to the bacteria ....OR..that the bacteria is getting worse somehow ( in effect getting worse)?

Lastly, my sinus condition still seems to be about the same...any thoughts? I would have thought that this would have cleared a bit by phase 3.

Just trying to understand........sorry if these questions seem simple minded or repetetive in nature. Thanks for your time and I appreciate the help very much.

Norman

 

Prof Trevor Marshall
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 Posted: Sun Jul 30th, 2006 09:27

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Norman, Please move these questions to your progress report discussion, it is not relevant to the discussion about Professor Zinkernagel's work.

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 Posted: Sun Jul 30th, 2006 11:49

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After reading this thread and reviewing the 1951 paper by Klieneberger-Nobel, can one assume that the viruses mentioned by Dr. Z and the L forms discussed by Klieneberger are the same pathogen? 

In other words, do viruses REALLY exist or are they L forms of bacteria? 

Sherry



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